Dermatitis, Dandruff, and Seborrhea

• This lecture covers the introduction to dermatitis, dandruff, and seborrhea.
• The lecture is meant to complement individual and group learning in Problem-Based Learning (PBL).

Learning Objectives

• Recognize the pathophysiology, etiology, epidemiology, and clinical presentation of atopic, irritant contact, and allergic contact dermatitis.
• Recognize the tools to assess patients with symptoms of dermatitis.
• Be able to differentiate between atopic, irritant contact, and allergic contact dermatitis, based on clinical presentation.
• Recognize clinical characteristics of moderate to severe dermatitis.
• Know when to refer patients with dermatitis.
• Describe the pharmacologic class, mechanism of action, and most common and serious adverse effects of pharmacologic agents used to treat dermatitis.
• Be able to recommend different pharmacologic and nonpharmacologic alternatives for managing dermatitis, considering a patient's specific factors and tolerability.
• Describe the factors impacting quality of life in patients with atopic and contact dermatitis.

Topical Corticosteroids

• It is important to memorize the generic names and potency categories of specific steroids mentioned in the case.
• Dosing frequency needs to be thoroughly understood

key Terminology

• Dermatitis is a non-specific term for inflammation of the skin and is defined as ["dermis" = skin] + ["itis" = inflammation].
• Eczema is a specific term for "an inflammatory skin condition that causes itchiness, dry skin, rashes, scaly patches, blisters and skin infections”.
• Atopy is a genetic predisposition for developing allergic diseases of immune system dysfunction like allergic rhinitis, asthma, and atopic dermatitis.
• All of these terms are distinct, yet often interchanged.

Eczema Types

• Includes Atopic, Contact, Dyshidrotic, Neuro-dermatitis, Nummular, Seborrheic, and Stasis.

Atopic Dermatitis (AD) Epidemiology & Etiology

• Atopic dermatitis is a very common, chronic condition that often begins in childhood and is often associated with other atopic conditions.
• The specific etiology is unknown, but several factors may play a role, like genetics, race, environment, socioeconomic status, and living situations.

Risk/Aggravating Factors

• Genetics
• Environmental Allergens like soaps, detergents, astringents, dust mites, moulds, pollens, and animal fur
• Climate
• Sweating
• Stress
• Diet
• Skin dysbiosis
• Irritant Exposure like Disinfectants, solvents, allergens, fabrics, and tight clothing/compression
• Itch-Scratch Cycle

Pathophysiology

• Impaired skin barrier, dysregulated immune system, and genetic and environmental susceptibility are all contribute to atopic dermatitis.
• The impaired barrier allows allergens to penetrate and sensitize the skin.
• Tissue damage affects the skin barrier further, leading to the skin becoming sensitized against self-proteins, called the autoallergic stage.
• The dysregulated immune system results in high IgE and eosinophils increase inflammation in the skin.
• Genetic variance occurs in skin reactivity, transepidermal water loss (TEWL), and ceramide (lipid) levels, which varies with race.
• Predisposition to atopy, exposure to allergens, dry/cold environments, and chronic conditions are also key factors
• Filaggrin protein deficiency, required to break down and form hygroscopic free amino acids, is essential to skin moisture

Prevention of Atopic Dermatitis

• Interventions to prevent onset may include excluding certain foods in pregnancy/lactation, exclusive breast milk for the first 3-4 months of life, hydrolyzed formula instead of cow's milk formula, probiotics in the mother and or the infant, daily emollient use in high risk infants and exposure to animals.

Acute vs. Chronic Dermatitis

• Acute dermatitis includes generalized Xerosis and diffuse erythema alongside oozing.
• Chronic dermatitis symptoms include red, dry, and scaly skin, poor demarcation, scaly plaques, excoriation, and lichenification.

Clinical Presentation

• Pruritis (itch) is the primary symptom.
• Diagnosis is clinical, based on intense itch + symptoms.
• In the acute stage symptoms are Xerosis, Erythema (patches, plaques), Papules, vesicles, Weeping/oozing/crusting, and Excoriations.
• Chronic stage includes Scaling of Patches and Plaques alongside Lichenification.
• Skin color affects presentation, with the rash being more brown or purple-tinged versus red.

Assessment

• Clinical diagnosis through observation.
• If no itch, the diagnosis is questionable.

Severity

• Severity scales are not typically needed and can mischaracterize disease in skin of color.
• Severity differentiators include infrequent pruritus or frequent pruritus with excoriations vs. persistent pruritus with excoriations
• Mild dermatitis has little to no impact on sleep, daily activities and well-being.
• Moderate dermatitis has moderate impact on sleep, daily activities and well-being.
• Severe dermatitis will major impact on sleep, daily activities and well-being.

When to Refer

• Severe symptoms
• Unresolved symptoms after 14 days of appropriate therapy
• Secondary infection
• Diagnosis unclear
• Palms and/or soles affected
• Suspected drug reaction

Goals of Therapy

• Main goals are to relieve symptoms like dry skin and pruritis, reduce inflammation and the number/severity of lesions, reduce the risk of complications and prevent flares, and preserve the quality of life.

Nonpharmacologic Treatment

• Identifying and Avoiding Individual Triggers
• Providing Education and Mental Health Support
• Clothing and Laundering
• Sports and Exercise
• Diet
• Dressings and wraps

Pharmacologic Therapies

• Bath Products like oils, salts, colloidal oatmeal, and soaps/cleansers
• Barrier/Protectant Products
• Moisturizers
• Tar Preparations
• Natural Health Products
• Topical Corticosteroids
• Systemic Corticosteroids
• Topical Calcineurin Inhibitors
• Topical Anti-Infectives
• Antihistamines

Bathing

• Needs to hydrate skin and remove crusts.
• Should be limited to 5-10 minutes maximum with warm water, and soapless cleansers should be avoided.

Treatment Overview

• Basic skin care (moisturizing) is critical at every stage.
• Trial interventions for 2-4 weeks before moving on and recall chronic conditions when patients are stable.

Moisturizers

• Classes: Emollients, Occlusives, Humectants, and Barrier Repair Agents.
• Formulations: Oils, Ointments, Creams, and Lotions.

Topical Corticosteroids

• First line and mainstay of treatment for chronic and acute dermatitis.
• Anti-proliferative, immunosuppressive, anti-inflammatory and vasoconstricting effects:

Potency

• Same steroid, with same concentration in different vehicles results in different potency.
• From most to least potent: clobetasol propionate 0.05% and betamethasone dipropionate glycol 0.05%, flucinonide 0.05% and betamethasone dipropionate 0.05%, hydrocortisone-17-valerate 0.2% ointment and betamethasone valerate 0.05%-0.1%, and hydrocortisone 0.5%, 1% and desonide 0.05%

Topical Corticosteroids: Selection

• Body Area, Skin Quality, Vehicle and Additives and individual Patient Factors all contribute.

Topical Corticosteroids: Finger Tip Units (FTU)

• 1 FTU ≈ 0.5 g
• 1 FTU covers 250 cm², or 1 adult hand with fingers closed.
• FTUs needed depends on area of the body and age of the patient.

Application

• Early, aggressive treatment (e.g., appropriate potency, twice daily, then twice weekly to maintain) mitigates longer/more potent future treatment.
• Steroid phobia is 'negative feelings and beliefs expressed by the public regarding the safety profile of topical corticosteroids".

Adverse Effects

• ≥ 1% of patients: Dryness, itching, burning, and irritation (more common)
• Less Common: Skin atrophy, Telangiectasia, Striae, Purpura, Hypopigmentation, Acneform or rosacea-like eruptions, Infection/masking of symptoms, Rebound dermatitis and systemic effects.
• tends to be permanent, but fades and often misinterpreted.

Topical Calcineurin Inhibitors

• Calcineurin has a role in T-cell activation which leads to an immune response.
• Calcineurin inhibitors are topical immunosuppressants with anti-inflammatory action and are more specific and targeted than corticosteroids.
• Typically second-line, but preferable in some situations when there is sensitive, thin skin (eyelids; anogenital areas), poor steroid response, use as steroid-sparing agents (adverse effects, long-term use) and need for relapse prevention (2-3x/week application).
• Pimecrolimus (Elidel) is a 1% cream that can be used in children 3 months and older and is indicated for mild-moderate atopic dermatitis.
• Tacrolimus (Protopic) 0.03% ointment is indicated for children 2 years and older and the 0.1% ointment is for adults 16 years and older, indicated for moderate-severe atopic dermatitis.

Topical PDE4 Inhibitor

• Crisaborole (Eucrisa) 2% ointment
• This medicatin can be used for mild-moderate(?) atopic dermatitis in patients 3 months and older.
• Reduces the production of inflammatory cytokines by increasing intracellular cAMP levels.
• Has shown improvement for pruritis and overall AD severity, and can be used on all areas of the body.

Systemic Agents (FYI)

• Systemic corticosteroids, Oral cyclosporine, Systemic immunosuppressants (e.g., methotrexate), and Biologic therapy (dupilumab) are generally used in severe/refractory cases.

Quality of Life

• This is an often-underappreciated aspect of atopic dermatitis and includes poor itch management, financial burden, reactions to food/allergies, and psychosocial impacts.

Role of the Pharmacist

• Monitor adherence, response to therapy, adverse effects
• Educate on proper use of medications, trigger minimization
• Dispel myths about steroids and calcineurin inhibitors
• Promote proper skin care, moisturizing
• Set expectations about the chronic nature of AD
• Assess & Prescribe/Refer as needed

Contact Dermatitis Etiology & Pathophysiology

• Inflammation in the skin resulting from contact with external stimuli. Irritant Contact Dermatitis (80% of contact dermatitis)
• Direct cytotoxic effects of irritants (NOT allergens)
• Innate immune system response
• Fast onset (hours)
• Allergic Contact Dermatitis (20% of contact dermatitis)
• Antigen-specific T-cell activation
• Previous sensitization required (adaptive immune system)
• Delayed onset (12-48 hours)

Clinical Presentation

• Allergic & Irritant: common presentation, making history critical.
• Itching, swelling, erythema, & scaling indicate contact dermatitis
• Skin response is dependent on chemical cause, duration/nature of contact, and individual patient factors/degree of susceptibility.
• Often see sharp demarcations/margins.
• Acute phase: Red, edematous papules turning into vesicles/bullae (may ooze).
• Irritant contact causes burning, stinging, and soreness.
• Allergic contact can include significant edema.
• Chronic phase: Primary lesions resolving results in dryness, lichenification, pigment changes, excoriations, and fissuring.

Risk/Aggravating Factors

• Sexual contact
• Impaired cell-mediated immunity (e.g., AIDS, lymphoma, atopic dermatitis)
• Ethnicity (generally more common in Caucasian race)
• Climate (cold, dry air)
• Exposure-related factors (Gender/aesthetic expression (products), Body site (often product-dependent), Occupation/leisure activities)

Treatment

• Trigger identification & avoidance
• History-taking. Basic skin care and Topical corticosteroids

When to Refer

• Spreads to distal sites
• More than 30% BSA affected
• Staying in acute phase longer than 2-3 days
• Chronic and non-responsive within 10 days
• Secondary infection suspected
• Interferes with quality of life

Differences

• Dandruff is a Limited to otherwise healthy scalp, with Limited or no erythema presenting with Silvery-gray scale
• Seborrheic Dermatitis is associated with Sebborheic areas (++ sebaceous glands) on the Scalp + eyelashes/brows, facial hair, Nasolabial, ear canal, behind ear, and Sternum, folds (breast, groin, etc.), and scaling.

Epidemiology & Etiology

• Dandruff: Uncommon in children, but affects ~50% of those over age 30 and is associated with a potential disequilibrium between fungal and bacterial parts of microbiome and/or an increase in Malassezia yeast.
• Seborrheic Dermatitis: Common in infancy and at ages 20-50 with Males > females.

Nonpharmacologic Treatment

• Avoid/stop triggers – drugs, stress, environment, diet
• Irritating products, long hair/facial hair, excessively hot water
• Cool mist humidifier
• Sunlight, warm weather
• Blepharitis: compresses, gentle scale removal
• Nonmedicated shampooing 3+ times/week , rinse thoroughly, dry hair

Pharmacologic Therapy

• Topical therapy is the 1st line (shampoos, lotions, creams, ointments); oral if needed (severe, recalcitrant disease)
• Treatment = Antifungal, Anti-inflammatory, and Keratolytics followed by Moisturizers for softening scale

Greater Efficacy Antifungals

• Azoles, such as ketoconazole as well as oral antifungals
• Topical antifungals should be used initially ~4x/week x 2-4 weeks and as maintenance ~1x/week

Less Efficacy

• Selenium sulfide and Zinc pyrithione

Severe Cases

• Systemic agents include -azoles and terbinafine.
• They may have ADRs and potential Drug interactions.
• Only available via Rx only

Other therapies

• Anti-Inflammatories: sx relief
• Topical Corticosteroids
• Topical Calcineurin Inhibitors, Add-on to other tx with topical calcineurin inhibitors instead of corticosteroids as needed

Monitoring

• Assess and monitor the following parameters:
• Scale thickness, Plaque thickness, Redness, Surface area involved, Extension to other sites or generalization.
• The following also need to be monitored: Scratching, Disruption of sleep/daily activities, Stress/anxiety/depression, Therapy progression, and Recurrent episodes
• These factors should decrease after therapy effectiveness.
• Note any Safety endpoints such as allergic reactions and severe dryness.
• Patients should monitor their conditions daily and healthcare providers can follow up within 2-3 weeks.